A popular argument for human evolution and our shared ancestry with apes has lost its steam in light of new genetics research at the Institute for Creation Research and a recently published article in a scientific journal.1 The research is related to the beta-globin pseudogene and shows it to be functional and important to hemoglobin gene regulation.

Hemoglobin is a protein in human red blood cells that transports oxygen. The hemoglobin protein is a cluster of two different protein chains. One of these chains is called the alpha-globin and remains similar in composition during human development. The second is called the beta-hemoglobin chain, which specifically changes in composition at the embryo-to-fetal transition and again at the fetal-to-adult transition. This allows the developing embryo-baby to receive oxygen at optimum levels.

The human beta-globin proteins are encoded by five genes inside a cluster of six genes on chromosome 11. The embryo-to-adult growth stage expression of each gene in the cluster depends on that specific gene’s interaction with a control region preceding the whole cluster called the locus control region or LCR.

While five out of the six genes in the beta-globin cluster produce proteins, one of the genes called HBBP1 does not because of several stop sequences in its code previously postulated to be mutations. This gene was classified as a pseudogene (a broken defunct remnant) because of its assumed non-functionality. Because the gene—along with its presumed errors—is also found in chimpanzees and gorillas, evolutionists claimed it as proof of inherited “shared mistakes” from an ape ancestor.

A key problem with this idea is the actual evidence for the claim. Evolutionists have wondered why, if the HBBP1 gene is non-functional, its DNA has not mutated significantly since no selection has been acting on it. The so-called evidence for common ancestry with this sequence actually argues against it. It also indicates that the HBBP1 gene may actually be functional and serving a common purpose in both humans and apes.

A recent report showed that the HBBP1 gene is highly non-variable within both human and chimpanzee populations.2 That same report also showed that the HBBP1 gene interacts with the LCR region and is highly functional. Shortly following this, another research paper was published indicating the HBBP1 gene exhibited the more genetic regulatory connections in the various regions of the globin-gene cluster than the other beta-globin genes.3

Inspired by these reports, I began a public DNA database mining project looking for more evidence of genetic function for the HBBP1 gene. The data were overwhelming! Multiple RNA transcript variants are produced by this gene that are thought to be involved with the regulation of beta-globin gene expression. The databases also showed that key regulatory proteins called transcription factors were binding to the HBBP1 gene and that the DNA surrounding the gene had all the telltale epigenetic marks of actively transcribed DNA, indicating that it was highly functional.4 Perhaps the most spectacular finding was data that showed the HBBP1 gene was expressed in at least 251 different human cell and/or tissue types.

In addition to the functional genomics data, my research uncovered three different recently published research reports showing that mutations in the HBBP1 gene caused various forms of a blood disease called beta-thalasemia. The data mining work also uncovered unpublished genetic information showing that mutations in the HBBP1 gene area may also be partial contributors to osteoarthritis.

Instead of being a useless genomic fossil according to errant evolutionary predictions, the HBBP1 beta-globin pseudogene is genetically active and plays a key functional role in the genome as a cleverly engineered feature programmed by God the Creator.